Physiology of Aging
Introduction
- Aging = complex, multifactorial; nutrition is major determinant from pre-conception onward.
- Key interactive domains: genetics, health behaviours, lifestyle/environment, medical conditions.
- TABLE 2-1 cross-links physiologic changes with nutrient needs. Selected examples:
- ↓ muscle mass → ↓ energy need + ↑ need for high-quality protein
- Atrophic gastritis, ↑ gastric pH → ↑ need for vitamins B6,B{12},K, folate, Ca, Fe, Zn
- ↓ skin vitamin D synthesis + renal activation → ↑ need for Ca & D.
- Normal/physiologic aging (senescence) ≠ pathology, yet reduces functional reserve → ↑ vulnerability to disease.
Theories of Aging
- Two broad, inter-connected categories:
- Programmed theories
- Life span genetically pre-set; cellular "biologic clock".
- Telomere shortening:
- Telomere = protective non-coding DNA cap; each replication shortens length.
- When too short → loss of chromosomal protection → apoptosis/senescence.
- Short telomeres correlate with shorter life span & ↑ chronic disease risk; heritable, longer in women.
- Error/Damage theories
- Cumulative environmental insults create cellular deterioration.
- Free-radical/ROS theory: mitochondrial respiration → ROS → DNA/protein/lipid oxidation → mutations, dysfunction, death.
The Role of Cell Replication & DNA Stability
- Accurate DNA replication (≈ 3\times10^{9} base pairs/cell division) essential for longevity.
- DNA repair proteins correct mismatches; capacity declines with age → mutation accumulation.
Genetics vs. Environment
- Centenarian data: avg. centenarian often in better health than avg. 80-yr-old.
- Lifespan variance ≈ 20–30 % genetic, 70–80 % environmental/epigenetic.
- Longevity-linked genes: PON1, FOXO variants, etc. interplay with diet, PA, BMI, smoking.
Epigenetics
- Epigenetics = heritable gene-expression changes without DNA-sequence alteration (e.g., DNA methylation).
- Methylation patterns correlate with "epigenetic age".
- Potential reversibility via diet, lifestyle → target for delaying age-related diseases.
Calorie Restriction (CR)
- Only universal life-span-extending intervention across species.
- Typical protocol: 15–40 % energy reduction without malnutrition.
- Mechanisms: slowed DNA methylation drift, lower oxidative damage, ↑ energy efficiency.
- Human RCT: 15 % CR × 2 yrs → ↓ resting metabolic rate & oxidative stress → supports "rate-of-living" theory.
- Research into CR mimetics (e.g., resveratrol, metformin, rapalogs).
Whole-Body Physiologic Summary (Table 2-2 highlights)
- ↓ lean body mass, ↑ adiposity until 60 y then fat ↓; drug distribution changes.
- ↓ dopaminergic receptors → parkinsonian traits.
- Sensory losses: presbyopia, presbycusis, taste/smell decline.
- ↓ renal blood flow & GFR; ↓ hepatic P-450; ↓ baroreflexes; ↓ vital capacity & ↑ residual volume.
Gastrointestinal Changes
- Oral health
- First signs of malnutrition show in oral tissues; xerostomia (often drug-induced) raises caries risk.
- Poor dentition/dentures → limited food choices, social withdrawal.
- Sensory decline
- Taste buds ↓ after 40–60 y; salty/sweet lost first. Olfactory impairment in 62–75 % ≥80 y.
- Consequences: anorexia of aging, over-salting, food safety issues.
- Esophagus
- Dysphagia prevalence 15–35 % elders; due to neuro diseases, sarcopenia, meds (opioids, anticholinergics).
- Complications: aspiration pneumonia, dehydration, weight loss.
- Stomach & SI
- Delayed gastric emptying → post-prandial hypotension, GERD.
- Atrophic gastritis + H. pylori ↑: ↓ HCl & IF → B_{12} malabsorption.
- Pancreatic enzyme output & bile ↓ → fat malabsorption & ADEK deficits.
- LI
- Transit slows; constipation common multifactorial (↓ fiber, fluids, mobility, meds).
Body Composition Changes
- Weight: rises till ~60 y then plateaus/declines.
- Sarcopenia: loss of muscle mass & strength (8–40 % ≥60 y; >50 % ≥75 y).
- Drivers: anabolic resistance, inactivity, inflammation, hormonal shifts, inadequate protein.
- Intervention: ≥1.0-1.2\,g\,protein\,kg^{-1}, leucine-rich sources, resistance training, antioxidants.
- Sarcopenic Obesity: coexistence of high fat + low muscle → compounded disability, insulin resistance.
- Intentional weight loss may exacerbate muscle loss—must combine with exercise + protein.
Cardiovascular & Respiratory Changes
- Cardiovascular aging
- Structural: arterial stiffening, endothelial dysfunction, LV wall thickening, ↓ max HR & VO2 max.
- Atherosclerosis develops over decades; influenced strongly by diet/PA.
- Modifiable dietary risk factors (Table 2-4)
- \uparrow SFA/TFA & cholesterol ↑ LDL; soluble fiber, sterols, MUFA/PUFA ↓ LDL.
- Excess refined CHO, ETOH, obesity ↑ TG & ↓ HDL.
- AHA 2020 ideal health metrics: smoke-free, BMI<25, PA ≥150 min/wk, DASH-like diet, optimal BP, lipids, glucose.
- Hypertension: pre-HTN 120\le SBP \le139\,mmHg or 80\le DBP \le89\,mmHg doubles risk → lifestyle & DASH.
- Lungs: ↓ elastic recoil, ↓ vital capacity, ↑ residual volume; immune decline ↑ pneumonia risk.
Renal System
- Peak renal mass in 40s; by 60 y average 25 % function lost.
- Annual GFR drop ≈ 0.75\,mL\,min^{-1}\,1.73m^{-2}.
- CKD defined as GFR < 60\,mL\,min^{-1}\,1.73m^{-2} ≥3 months.
- Contributors: diabetes, HTN, CVD, obesity, nephrotoxic drugs.
- Aging GU tract: bladder capacity ↓, prostate hypertrophy, pelvic floor laxity → incontinence → voluntary fluid restriction → dehydration.
Skeletal Health
- Peak bone mass ~late 20s; 50–90 % genetically set, remainder diet + activity.
- Hormonal regulators: PTH, calcitonin, GH/IGF-1, cortisol, vitamin D.
- Vitamin D synthesis ↓ in skin & renal activation; combined with low intake → poor Ca absorption.
- Osteoporosis
- Microarchitectural deterioration; common fracture sites spine, hip, wrist.
- Primary (age/post-menopause) vs Secondary (drugs e.g., glucocorticoids, PPIs).
- Nutrition essentials (Table 2-7): Ca 1200\,mg/d, vitamin D 800–1000\,IU/d, vit K, Mg, protein (but not excessive), ω-3, antioxidants.
- Excess Na, P (cola), vitamin A, alcohol, caffeine can leach bone.
- Weight-bearing & balance exercise reduce falls—the largest fracture modulator.
Immune, Nervous, Endocrine, Hematologic Changes
- Immunosenescence
- ↓ naïve T & B cells, ↓ vaccine response, ↑ inflammatory cytokines.
- Nutrition link: deficits in protein, vitamins A, C, D, E, B6, B{12}, folate, Zn, Se impair immunity; probiotics & ω-3 may modulate.
- Moderate PA boosts adaptive immunity.
- Nervous system
- Brain volume ↓, neurotransmitter synthesis ↓; slower processing, sensory losses.
- Nutrients impacting cognition/mood: B-complex (folate, B6,B{12}), vit D, ω-3 (DHA), antioxidants (vit C, E, carotenoids).
- Endocrine
- ↓ sex steroids, GH/IGF-1, thyroid hormones; ↑ insulin resistance.
- Influence on sarcopenia, osteoporosis, metabolic syndrome.
- Anemia in Elders
- Prevalence >20 % ≥85 y. Three equal etiologies:
- Nutritional (Fe, B_{12}, folate)
- Anemia of inflammation/CKD/chronic disease (hepcidin-mediated Fe sequestration)
- Unexplained (possible cytokine or other micronutrient effects)
- Iron-deficiency often due to occult GI bleed.
- Work-up includes diet review, meds (acid suppressors), renal function; treatment may require combined nutrition + medical approaches.
Practical / Food-Service Perspectives
- Culture-Change movement → resident-directed meals, liberalized diets, restaurant-style menus, CDM oversight.
- Danger of over-restrictive diets (e.g., low Na) in elders: palatability ↓ → unintended weight loss & malnutrition.
- Need individualized, least-restrictive approach.
- LET’S DISCUSS exercises: beverage sugar cube demo; curate credible senior health websites; craft social-media messages.
Key Study Data & Numbers
- Centenarians worldwide 2015 ≈ 5\times10^{5}; projected 2050 3.7\,million.
- US centenarians up 43.6 % 2000–2014 (50,281 → 72,197).
- Immunologic decline starts ≈50 y; olfactory loss in 62–75 % ≥80 y.
- Dysphagia prevalence 15–35 % institutional elders; 11.4 % community dwelling.
- Obesity in ≥65 y: >30 %; Sarcopenia affects 8–40 % ≥60 y.
Ethical / Practical Implications
- Balancing disease-oriented restrictions with quality of life; respect autonomy (culture change).
- Equity in access: socioeconomic & functional barriers to nutrient-dense foods.
- Research gaps: epigenetic diet modulation, CR mimetics, anemia of unexplained origin.
Connections to Foundational Principles
- Homeostasis: Aging reduces reserve → nutrition acts as buffer.
- Rate-of-Living & oxidative stress theories linked to antioxidant nutrient needs.
- Systems biology: gastro, renal, hepatic, endocrine interact—drug/nutrient interplay.
Formulae & Clinical Cut-offs (selected)
- Telomere attrition per mitosis \approx 50–200\,bp
- CKD: \text{GFR}
- Pre-HTN: 120\le SBP<140 mmHg OR 80\le DBP<90 mmHg.
- Protein for sarcopenia: 1.0–1.2\,g\,kg^{-1}\,day^{-1} (may ↑ to 1.5 g in illness).
- Calorie restriction research range: 15–40\,\% energy deficit.
Key Terms (as per chapter)
- Senescence, Dysphagia, Dyspepsia, Gustatory dysfunction, Olfaction, Immunosenescence, Sarcopenia, Sarcopenic obesity, DNA methylation, Epigenetics.